Evolution of the human lifespan and diseases of aging: Roles of infection, inflammation, and nutrition

Abstract

Humans have evolved much longer lifespans than the great apes, which rarely exceed 50 years. Since 1800, lifespans have doubled again, largely due to improvements in environment, food, and medicine that minimized mortality at earlier ages. Infections cause most mortality in wild chimpanzees and in traditional forager-farmers with limited access to modern medicine. Although we know little of the diseases of aging under premodern conditions, in captivity, chimpanzees present a lower incidence of cancer, ischemic heart disease, and neurodegeneration than current human populations. These major differences in pathology of aging are discussed in terms of genes that mediate infection, inflammation, and nutrition. Apolipoprotein E alleles are proposed as a prototype of pleiotropic genes, which influence immune responses, arterial and Alzheimer's disease, and brain development.chimpanzee | pathology H umans have the longest life spans of any primate. Even under the conditions of high mortality experienced by hunterforagers, the human life expectancy at birth (LE 0 ) is twice that of wild chimpanzees. This inquiry considers the demographics and pathology of aging in humans and great apes as an approach to understanding how aging processes evolved with longer lifespans. I argue that immune functions and nutrition have been of major importance in the evolution of aging and longevity.

How grandmother effects plus individual variation in frailty shape fertility and mortality: Guidance from human–chimpanzee comparisons

“…These decreases in mortality and fertility typify changes in some other populations at about the same time, likely due to improvements in nutrition, sanitation, and medicine (21,101). By the end of the 20th century, continuing decreases in fertility and increases in juvenile and adult survival resulted in life expectancies double those of most historical and ethnographic populations (1,9,102). The increases in survival allowed increased heterogeneity at older ages.…”

ApoE genotype: from geographic distribution to function and responsiveness to dietary factors

“…The apoE protein is produced in various tissues with particular high concentrations in liver, brain, kidney, lymphocytes and adipose tissue. Beyond its known function in lipid and cholesterol metabolism apoE is believed to modulate many aspects of ageing in brain and artery walls (5) .…”

The endocannabinoid system in normal and pathological brain ageing

“…Normal, healthy brain ageing is associated with an increased number of activated microglia [125][126][127] and with an enhanced level of pro-inflammatory cytokines. The increased pro-inflammatory environment in the brain accelerates brain ageing [128,129], aggravates cognitive deficits impairing neuronal functions [130][131][132] and reduces neurogenesis [133,134]. Activated microglia can be both anti-inflammatory (which supports the neurons) and pro-inflammatory (which damages neurons).…”